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Gastric ulceration due to chronic mesenteric ischaemia treated by stenting of the inferior mesenteric artery
  1. V K Patel1,
  2. I Barrison1,
  3. J Jackson2,
  4. S Catnach3
  1. 1Hemel Hempstead General Hospital, Hemel Hempstead, Hertfordshire, UK
  2. 2Hammersmith Hospital, London, UK
  3. 3Hemel Hempstead General Hospital, Hemel Hempstead, Hertfordshire, UK
  1. Correspondence to:
    Dr S Catnach
    Hemel Hempstead General Hospital, Hillfield Rd, Hemel Hempstead, Hertfordshire HP2 4AD, UK; susan.catnach{at}whht.nhs.uk

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We report a case of gastric ulceration due to visceral ischaemia treated successfully by stenting of the inferior mesenteric artery (IMA) alone. Gastric ulceration has very rarely been described as a result of chronic mesenteric ischaemia.[1–3] Four of the five cases described in these reports were treated surgically and one by angioplasty to the superior mesenteric artery (SMA). All were reported to have successful resolution of gastric ulcers. To our knowledge, there is no other case of successful stenting of the IMA alone, with resolution of gastric ischaemia described in the medical literature.

Our patient was a 50 year old woman presenting with abdominal pain, loss of appetite, vomiting, and weight loss. Pain was maximal in the epigastrium and precipitated by meals. Apart from being a smoker there was no other significant medical history. She was empirically started on omeprazole. Oesophagogastroduodenoscopy (OGD) revealed multiple serpiginous ulcers affecting the body of the stomach with extension to the cardia (fig 1D). Histology from the ulcers demonstrated ulceration with regenerative hyperplasia with no evidence of Helicobacter pylori infection. An abdominal computed tomography scan showed non-specific thickening of the pylorus and first part of the duodenum but was otherwise normal. A small bowel follow through revealed no abnormality.

Figure 1

 (A) Inferior mesenteric artery (IMA) stenosis, (B) superior mesenteric artery occlusion, (C) stented IMA, and (D) gastric ulcer.

Fasting gut hormone levels, including gastrin level, after stopping omeprazole were normal and a vasculitis screen (including serum ANCA) was negative.

Her abdominal pain was controlled by morphine 120 mg/day. A repeat OGD 10 weeks after treatment with omeprazole 40 mg once daily showed continuing ulceration with no improvement since the previous examination. Further histology showed similar findings as before.

Abdominal angiography demonstrated complete occlusion of the SMA origin (fig 1B), and tight ostial stenoses of the IMA (fig 1A) and coeliac axis. The SMA branches filled sluggishly and were reconstituted almost exclusively via the left colic branch of the IMA.

Attempts to bypass the coeliac axis stenosis and proximal SMA occlusion were unsuccessful. The IMA was catheterised; initial pressure measurements demonstrated a mean IMA pressure of 20 mm Hg (mean pressure gradient between the IMA and the aorta of 70 mm Hg) which persisted after angioplasty with a 5 mm balloon. A 5 mm diameter, 16 mm long balloon mounted stent was therefore placed across the ostial stenosis (fig 1C) resulting in marked improvement of the angiographic appearance and almost complete obliteration of the mean pressure gradient. The patient was commenced on aspirin and warfarin and an international normalised ratio of 2 was maintained. She was weaned off the opiate analgesia and was discharged on omeprazole, aspirin, warfarin, and amitriptyline.

Her symptoms resolved completely and amitriptyline and warfarin were discontinued three months later. A repeat OGD showed complete healing of the ulcers. She was continued on aspirin 150 mg and omeprazole 10 mg daily and advised to stop smoking, but unfortunately was not successful in doing so. She has been followed up for 18 months and has had no recurrence of her symptoms.

The interest in this case lies in the fact that only the IMA needed to be stented to achieve an appropriate vascular supply to the stomach, despite severe occlusions and reduced flow in the coeliac and mesenteric axes. This has not been described before, and demonstrates that minimally invasive radiological stenting of only one territory of the mesenteric axis, even the IMA alone, can provide enough blood flow to treat the complications of chronic mesenteric vascular disease. This case is a reminder that chronic mesenteric vascular disease should be considered as a cause of resistant gastric ulceration. This case also demonstrates that minimally invasive radiological stenting of only one territory of the mesenteric axis, even the IMA alone, can provide enough blood flow to treat the complications of chronic mesenteric vascular disease.

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Footnotes

  • Conflict of interest: None declared.

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